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I've been hearing a lot of people recently who claim that having good cardiovascular fitness (i.e. frequent aerobic workouts) actually makes the immune system "healthy" and therefore means that the MS will run a more benign course. Is this true? It seems a bit illogical though. Howcome athletes who exercise regularly everyday still get MS? Howcome some of these athletes, despite remaining active, end up in a wheel chair? Does this not disprove this theory?
Joined: Jul 28, 2004 Posts: 128 Location: Michigan, USA
Posted: Thu Apr 07, 2005 5:43 am Post subject: Exercise
Kae63,
I too have heard that and read that. I'm on one of the ABC's, even the newsletter recommmends a "healthy lifestyle.
Direct quote:
" Medication is an important part of MS therapy, but is by no means the only weapon people have in the fight against MS. A focus on exercise and proper nutrition can have a positive and lasting effect in people with MS."
One of the points that is always brought up is not to overheat yourself. Personally, this has never bothered me. I have a hot tub and am able to sit in it without any increase in symptoms. Increasing core body temp. definitely has an adverse affect on many people with MS. My Neuro. says it can aggravate symptoms, but doesn't have any lasting effects such as making your MS worse.
I guess, how could a sensible, mild to moderate exercise program not help anyone?
As far as the athletes, exercise is not a preventative, has never been shown to cause, or cure MS. I'd say it just falls into that "healthy lifestyle" category that is sensible for everyone MS or not.
Posted: Tue Apr 12, 2005 9:15 am Post subject: My opinion about the exercise/MS theories...
My opinion is, that exercise that produces endorphins would help. Now that I have researched LDN and have taken it for 3 years I truly believe that is the answer to exercise and MS. That is the mechanism behind the LDN therapy, endorphin production. Not all exercise creates endorphins. This is what I truly believe saved me from a lot of attacks for over 10 years. I was an avid aerobicizer...is that a word?..lol. Anyway, I started to go downhill once I started to slack off of the regular aerobic exercise. I was still active like bike riding and such but I was no longer pumping out those endorphins as I had and I started to have new symptoms...etc. I started the LDN and have since gone back to the way I was prior to the LDN. I have some residual permanent damage that will be with me until maybe stem cell therapy is approved but all in all not bad at all. I plan to stay with the LDN until perhaps stem cell therapy. Pretty sure I would not need any other therapy at this point in time.
Several years ago I attended a seminar given by Fred H. Gage of the Salk Institute. He discussed that mice given a running wheel in their cage and allowed to freely exercise had a greater number of stem cells produced in the brain than mice which did not have the running wheel available. He also stated that the fate of the stem cells was controlled by their environment, i.e., the other cell types surrounding the new cells, and that they could form into either neurons or oligodendrocytes.
I've listed some papers below which should provide a review of the material. However, I should note that there are many more papers from Fred H. Gage available via PubMed.
Running increases neurogenesis in the dentate gyrus of the hippocampus, a brain structure that is important for memory function. Consequently, spatial learning and long-term potentiation (LTP) were tested in groups of mice housed either with a running wheel (runners) or under standard conditions (controls). Mice were injected with bromodeoxyuridine to label dividing cells and trained in the Morris water maze. LTP was studied in the dentate gyrus and area CA1 in hippocampal slices from these mice. Running improved water maze performance, increased bromodeoxyuridine-positive cell numbers, and selectively enhanced dentate gyrus LTP. Our results indicate that physical activity can regulate hippocampal neurogenesis, synaptic plasticity, and learning.
New neurons are continually generated in the adult hippocampus, but the important question, whether adult neurogenesis is transient or leads to the lasting presence of new neurons, has not yet been answered. Dividing cells were labeled with bromodeoxyuridine (BrdU) and were investigated by means of immunofluorescence and confocal microscopy at several time-points 1 day to 11 months thereafter. BrdU-labeled neurons remained stable in number and in their relative position in the granule cell layer over at least 11 months. This finding implies that the addition of new neurons is not transient and that their final number and localization are determined early. By contrast, expression of immature markers beta-III-tubulin and doublecortin in BrdU-labeled cells, peaked early after division and was not detectable after 4 weeks. In transgenic mice expressing enhanced green fluorescent protein under the nestin promoter none of the BrdU/nestin-positive cells early after division expressed the mature marker NeuN, confirming that no dividing neurons were detected. These new data suggest that new neurons are recruited early from the pool of proliferating progenitor cells and lead to a lasting effect of adult neurogenesis.
New cells are continuously generated from immature proliferating cells throughout adulthood in many organs, thereby contributing to the integrity of the tissue under physiological conditions and to repair following injury. In contrast, repair mechanisms in the adult central nervous system (CNS) have long been thought to be very limited. However, recent findings have clearly demonstrated that in restricted areas of the mammalian brain, new functional neurons are constantly generated from neural stem cells throughout life. Moreover, stem cells with the potential to give rise to new neurons reside in many different regions of the adult CNS. These findings raise the possibility that endogenous neural stem cells can be mobilized to replace dying neurons in neurodegenerative diseases. Indeed, recent reports have provided evidence that, in some injury models, limited neuronal replacement occurs in the CNS. Here, we summarize our current understanding of the mechanisms controlling adult neurogenesis and discuss their implications for the development of new strategies for the treatment of neurodegenerative diseases.
Joined: Jul 28, 2004 Posts: 128 Location: Michigan, USA
Posted: Thu Apr 14, 2005 6:54 am Post subject: Exercise
Based on the lastest posts on this thread, how would you explain this?
Joyce wrote:
Quote:
My opinion is, that exercise that produces endorphins would help. Now that I have researched LDN and have taken it for 3 years I truly believe that is the answer to exercise and MS. That is the mechanism behind the LDN therapy, endorphin production. Not all exercise creates endorphins.
So is it the LDN or the exercise?
Coincidentally, I just received a PM from one of the other members here. It is like a copy of this latest public thread w/ regard to LDN and exercise. There again, I must ask her, exercise or LDN?
Many times I've read about the correlation between latitude/season and MS. Generally, those of us in northern latitudes get less exercise in winter months. Certainly we get less sunlight(bring in the Vitamin D component). Connection?
NHE's quotes raise really good points, none of them directly relate endorphins to the benefits, but they show the benefits of exercise though.
These latest posts have sparked my interest in LDN. Is this something available in the US? Considered a novel therapy? Certainly not mainstream. I had never even heard of it before reading about it here on this forum.
Posted: Thu Apr 14, 2005 10:04 am Post subject: My story...
Hi,
Finally had a chance to log on and respond to this. I am no longer able to exercise the way I did in those days when I think I was preventing attacks because I am no longer able to keep up with a class such as I was doing then, which was generally an hour long step class where I'd be sweating. I can still do step slowly but no longer can keep up with an actual class. I started to slack off of the exercise and would go when I felt like it and not consistently the way I had up to that point, which was at least 3 days a week. I started to go downhill with legs that were numb from the knees down and strange new optic problems for a good 4 to 6 months. After that, I have permanent damage that prevents me from walking long distances and my balance is off. That is when I started on my search for something to slow progression. It was all I could have hoped for at that point. I started taking LDN daily in May of 2000 and that causes my body to create lots of endorphins for me now, since I am no longer able to do the type of exercise that would produce endorphins. I do still exercise now but it is more weight machines and not heart pumping sweat/endorphin producing exercise. I think that if I would not have slacked off about 4 or 5 years ago, I'd still be maybe about 90% today possibly with no permanent damage.
Of course I am not a doctor or an expert, just an MS patient relaying her experiences. I have had no further progression since starting the LDN and I look forward to meeing Dr. Bihari this June in New York at the LDN conference. Am also looking forward to meeting all of you that plan to attend.
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